The Altenberg Sixteen

_{Paul Nelson

March 4, 2008

Intelligent Design}

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HT to Larry Moran’s Sandwalk for the link to this fascinating long piece by journalist Suzan Mazur about an upcoming (July 2008) evolution meeting at the Konrad Lorenz Institute in Altenberg, Austria.

“The Altenberg 16” is Mazur’s playful term for the sixteeen biologists and theoreticians invited by organizer Massimo Pigliucci. Most are on record as being, to greater and lesser degrees, dissatisfied with the current textbook theory of evolution. Surveying the group, I note that I’ve interacted with several of the people over the years, as have other ID theorists and assorted Bad Guys. This should be an exciting meeting, with the papers to be published in 2009 by MIT Press.

Mazur’s article is worth your attention. Evolutionary theory is in — and has been, for a long time — a period of great upheaval. Much of this upheaval is masked by the noise and smoke of the ID debate, and by the steady public rhetoric of major science organizations, concerned to tamp down ID-connected dissent. You know the lines: “Darwinian evolutionary theory is the foundation of biology,” et cetera.

But the upheaval is there, and increasing in amplitude and frequency.

[Note to Kevin Padian: journalists don’t like it when you do this to them. Mazur writes:

Curiously, when I called Kevin Padian, president of NCSE’s board of directors and a witness at the 2005 Kitzmiller v. Dover trial on Intelligent Design, to ask him about the evolution debate among scientists –- he said, “On some things there is not a debate.” He then hung up.

That hanging-up part…not so wise. If you’re going to say there’s no debate, explain why.]

Comments

Allan_MacNeill:
On the contrary, the problem of the origin of life has virtually nothing to do with evolutionary biology.
This is a cop out! Ever since it finally dawned on the OOL community that the first self-replicating organism wasn't DNA based, a huge chunk of pre-DNA life is solidly the responsiblility of the evolutionary biologist to figure out. Either the first self-replicating life actually was DNA based, and therefore was an act of creation, or there is an evolutionary path from simple replicator to DNA based life. If the latter, then it is the responsibility of the evolutionary biology community to figure out at least a feasible path. The fact that much has been lost in such ancient history may well make it impossible to determine whether the hypothetical path is the path that nature chose, it still is the responsibility of the evolutionary biologist to figure out if, and where, such a path exists. I reject the "its not my issue" argument on this one.bFast_{March 9, 2008
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Dr. MacNeill, I am well aware of your 47 models of variation. In fact I mention them quite frequently. I don't claim to understand all of them but I bet if each was explained in lay terms, it would be easy to know what to look for in changes in the genome and in the subsequent expanded gene pool. However, what are the documented cases of variation creation by these 47 methods and the species creation they led to. I realize all may have happened but what has been the pay out. Have there been any instances of novelty creation by any of these processes? Which of these processes would lead to bats and their sonar, birds and their wings, giraffes and their special blood pressure system, birds and their special oxygen delivery system, mammals and their four chambered hearts and warm bloodiness, humans and their long childhood development. I have read Sean Carroll's book and diid not find anything that pointed to any source of variation that would lead to the complexity we see. It is an interesting book. At one point he mentioned that it would take 10,000 pages of small print to list the instructions on how to make a human. Breath taking complexity. He explained how the complexity in a species probably happens during gestation but not why or how the system to do this came about other than speculation. I find evo devo as supportive of ID because it has to resort to incredible complexity to explain just how it works, but cannot really explain how everything arose. Other than to beg the question and point to some magical unknown species that preceded the Cambrian Explosion that had the Hox genes, Pax genes and other tools that led to everything. Nearly all of Behe's Irreducible Complexity examples arose during the Cambrian Explosion or in the magical unknown creature. Thanks for taking all the time to answer our queries. If you have tine, look at the thread on gene expression and comment if appropriate. There is not much debate going there but there are attempts to try to understand what controls gene expression and epigenesis has been mentioned and discussed a little.jerry_{March 9, 2008
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J: Thanks for the quote from Dr. Dembski. Precisely my point, and stated better than I could have.Allen_MacNeill_{March 9, 2008
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Again, note that mutations in hox genes such as FOX2P and BMP4 cause surprisingly large phenotypic changes, a phenomenon totally unanticipated by the "modern evolutionary synthesis." This, again, is why I have asserted that the "modern synthesis" (sometimes referred to as neo-Darwinism) has been replaced by a much more robust and empirically grounded theory explaining the major features of what Darwin called "descent with modificati — in a word, evolution.Allen_MacNeill_{March 9, 2008
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And here's one on BMP4: http://www.nature.com/hdy/journal/v94/n2/full/6800618a.htmlAllen_MacNeill_{March 9, 2008
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Here's a reference for FOX2P: Nature Posted: 22 August 2002 Title: Molecular evolution of FOXP2, a gene involved in speech and language Summary: Two normal copies of FOXP2 are necessary for language articulation. Alterations in amino acid sequence and nucleotide polymorphisms implement FOXP2 selection for human evolution. The gene encodes a protein of 715 amino acids and is classified as a forkhead transcription factor. Only three amino acids differ between comparisons of human and mouse FOXP2. Two of the three amino-acid differences between humans and mice occurred on the human lineage after the separation from the common ancestor with the chimpanzee. A change in amino acid 325 suggests a potential site for phosphorylation by a protein kinase. A study of 91 individuals revealed only one discrepancy in amino acid sequence. Researchers hypothesized that the gene is responsible for orofacial movements. They hypothesize that the gene may be responsible for the expansion of modern humans.Allen_MacNeill_{March 9, 2008
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Sorry; the link that I posted to chapter 14 of the Origin of Species was incorrect. Here is the correct link: http://darwin-online.org.uk/content/frameset?itemID=F373&viewtype=side&pageseq=477Allen_MacNeill_{March 9, 2008
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DLH wrote: "Without abiogenesis, Darwinism has no foundation to stand on." Untrue. Once again, virtually none of the theories of evolutionary biology depend in any way on the resolution to the question of the origin of life. Daniel Dennett pointed this out in Darwin's Dangerous Idea when he pointed out that Darwin "started out in the middle" by proposing a theory for descent with modification (what we now call "evolution") and the origin of of adaptations. His proposal did not address the origin of life at all, as a brief rereading of the summary of his argument in chapter 14 of the Origin of Species indicates: http://darwin-online.org.uk/content/frameset?itemID=F373&viewtype=side&pageseq=1 Again, I agree with Jerry: disputes over the origin of life are diversions from the real questions about descent with modification and the origin of adaptations, which were and are the core subjects of the theories of evolutionary biology.Allen_MacNeill_{March 9, 2008
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DLH wrote: "OOL is Darwinism’s Achilles heel." On the contrary, the problem of the origin of life has virtually nothing to do with evolutionary biology. Darwin did not mention it directly in any of his published works, and never speculated publically on the subject at all. My own position on this problem is that, given the immensely long period of time that has elapsed since the origin of life, the rocks that were formed during this period no longer exist at the Earth's surface (they are either buried so deeply as to be inaccessible, or have been destroyed by tectonic subduction). Furthermore, molecules do not fossilize, and so speculation about the chemical origins of life will always remain precisely that: speculation, unsupported by direct empirical evidence. As all of the participants in my summer seminar on evolution and design at Cornell agreed (including the ID proponents), the question of the origin of life has virtually no bearing on the origin of phenotypic variation or mechanisms of descent with modification, both of which are the core of evolutionary biology. Indeed, even the ID proponents in the seminar agreed that "Darwinism" (i.e. the theories proposed by Darwin himself, and modified by evolutionary biologists since then) are not affected in any way by the debate over the origin of life, nor will they be if this debate is ever resolved on the basis of future empirical discoveries. Therefore, I agree with Newton: "I make no hypotheses", and do not address questions of the origin of life as an evolutionary biologist.Allen_MacNeill_{March 9, 2008
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kairosfocus wrote: "Then, there is no credible evolutionary materialist mechanism for the onward origination of the diversity of body plans we see today and in the fossil record." Untrue. Sean Carroll's book, Endless Forms Most Beautiful contains a concise and lucid description of precisely this process, supported by a growing mountain of empirical data.Allen_MacNeill_{March 9, 2008
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Kairosfocus wrote: "...mutations of the kind that macroevolution doesn’t need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don’t occur." Not true. Indeed, mutations in hox genes are well known, and are the basis for many emerging models of major phenotypic change. For example, a mutation in the FOX2P hox gene (mostly inactivating it) is one of the primary reasons for the phenotypic anatomical and functional differences between humans and chimpanzees (and all other primates). Another mutation in another hox gene (BMP4) also contributed to the evolution of human vocal apparatus, shortening the muzzle and modifying the attachment points of the muscles used in speech. Also, it is interesting to note that both of these mutations inactivated the original functions of these genes, rather than "enhancing" them. They were, in other words, deleterious mutations, which nevertheless set the stage for the evolution of human speech.Allen_MacNeill_{March 9, 2008
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Jerry wrote: "No natural source of variation has ever been demonstrated. Without a source of variation, natural selection and sexual reproduction might be very sterile processes." As I pointed out recently at my blog, we now know of at least 47 major natural sources of phenotypic variation: http://evolutionlist.blogspot.com/2007/10/rm-ns-creationist-and-id-strawman.htmlAllen_MacNeill_{March 9, 2008
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William A. Dembski, The Design Revolution (2004), pp. 41-43:
Intelligent design needs to be distinguished from creation science or scientific creationism. The most obvious difference is that scientific creationism has prior religious commitments whereas intelligent design does not. Scientific creationism is commited to two religious presupositions and interprets the data of science to fit those presuppositions. Intelligent design, by contrast, has no prior religious commitments and interprets the data of science on generally accepted scientific principles. In particular, intelligent design does not depend on the biblical account of creation. The two presuppositions of scientific creationism are as follows: • There exists a supernatural agent who creates and orders the world. • The biblical account of creation recorded in Genesis is scientifically accurate. ... Proponents of scientific creationism treat the opening chapters of Genesis as a scientific text and thus argue a literal six-day creation, the existence of a historical Adam and Eve, a literal Garden of Eden, a catastrophic world-wide flood and so on. Scientific creationism takes the biblical account of creation in Genesis as its starting point and then attempts to match the data of nature to the biblical account. Intelligent design, by contrast, starts with the data of nature and from there argues that an intelligent cause is responsible for the specified complexity in nature... Scientific creationism's reliance on narrowly held prior assumptions undercuts its status as a scientific theory...
j_{March 9, 2008
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dennis grey From the second link in the main post, see: fascinating long piece by journalist Suzan Mazur about an upcoming (July 2008) evolution meeting at the Konrad Lorenz Institute in Altenberg, Austria.DLH_{March 9, 2008
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Mr. Nelson, Can you say where the link to the actual Sandwalk blog post is? sincerely, d. greydennis grey_{March 9, 2008
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Jerry at 165
“We all understand the OOL problem more or less but the issue here in this thread is the mechanism for change of multicellular life.”
Do we? Does anyone? OOL is Darwinism’s Achilles heel. You would do well to heed kairosfocus in reemphasizing it. Without abiogenesis, Darwinism has no foundation to stand on.
“Some others have introduced Sanford’s ideas which are YEC ideas and as such should receive special scrutiny before they are accepted.”
Are they? Dig into his work and I think you will find his arguments are based on works published by evolutionists - and are independent of YEC. Yes Sanford’s OOL model will be used to try to dismiss those arguments. And obviously Sanford would see such evidence as supportive of his origin ideas. But foundationally, he takes evolutionists models and shows that they disprove the Primary Axiom. Do NOT dismiss Sanford. I believe the flood of genetic evidence on mutations will be the quantitative data that drowns evolution. And thus Sanford’s collection of evolutionists models is very important for that.
“Second, this is not a site for Evangelicals to press their religious views as science.”
Check your presumptions or impressions vs the data. I showed you recorded data with supporting evidence from numerous ancient royal genealogies, not my beliefs, (of which you know little.)
“will continue to dispute any claims using the bible as scientific evidence“
That exposes your bias. Look at the data separate from your colored glasses. The majority of all 18th and 19th century objections to the bible have been refuted by archeological evidence.DLH_{March 9, 2008
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kairosfocus, Two things. First, this discussion is about the modern synthesis and what may replace it and has nothing to do with OOL. We all understand the OOL problem more or less but the issue here in this thread is the mechanism for change of multicellular life. Dr. MacNeill shed some light on the objections to the modern synthesis by many evolutionary biologists and a lot of the discussion has revolved around that. Some others have introduced Sanford's ideas which are YEC ideas and as such should receive special scrutiny before they are accepted. Second, this is not a site for Evangelicals to press their religious views as science. If they want to it is up to the moderators to say it is ok or not but I will continue to call the science as I see it and will continue to dispute any claims using the bible as scientific evidence for either biology or cosmology. To me it perverts the basic objectives of this site. Read the manifesto in the upper right hand corner and substitute " fundamentalist religious" for "materialist" and see if the essence of this declaration changes much. Many here do not agree with me when I say that I believe the YEC's are a problem for ID credibility. Where I live fundamentalist Christians especially YEC's are very suspect. And I am being kind with that description of people's attitudes toward their beliefs. Now they have the right to say "we don't care" but I am talking about decent religious people who hold these views. I have no problem with DLH's article on the archeological findings recently in Jerusalem and await what they find with further excavation. But I believe that wishful thinking driven by ideological reasons will never replace hard evidence. I am as tough on the Darwinists as I am on others who use ideology to advance their position. I object to Darwinists, YEC's and TE's because each uses religion or religious like motivation to justify their science. And this is supposed to be a site for science. Do you care if I offend the Darwinists here because I press then on the basis of their beliefs? If not then you should not care if I offend those who let religion rule their beliefs about science either. To me they are guilty of the same sin.jerry_{March 9, 2008
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DLH, Allen, Jerry et al: I have observed the back-forth over the past few days. It is clear that, while the discussion on Sandford's genetic entropy thesis and associated questions over mutation rates is an interesting one, it is largely a side-issue. For, the real "elephant in the middle of the room" is how we get TO the genomes and epigenetics that allow for the sort of system that is being perturbed by mutations. First, at origin of life. For that, let Leslie Orgel speak, even from beyond the grave (noting that the same objection obtains for his own favoured RNA world type scenarios, as Shapiro pointed out in his own earlier Sci Am article):
Theories of the origin of life based on metabolic cycles cannot be justified by the inadequacy of competing theories: they must stand on their own . . . . The prebiotic syntheses that have been investigated experimentally almost always lead to the formation of complex mixtures. Proposed polymer replication schemes are unlikely to succeed except with reasonably pure input monomers. No solution of the origin-of-life problem will be possible until the gap between the two kinds of chemistry is closed. Simplification of product mixtures through the self-organization of organic reaction sequences, whether cyclic or not, would help enormously, as would the discovery of very simple replicating polymers. However, solutions offered by supporters of geneticist or metabolist scenarios that are dependent on “if pigs could fly” hypothetical chemistry are unlikely to help . . .
Then, as Meyer aptly pointed out [and as was cited at 90 above], at body-plan level biodiversity [bearing in mind that the Cambrian "revolution" shows body plans "first" in the record]:
One way to estimate the amount of new CSI that appeared with the Cambrian animals is to count the number of new cell types that emerged with them (Valentine 1995:91-93) . . . the more complex animals that appeared in the Cambrian (e.g., arthropods) would have required fifty or more cell types . . . New cell types require many new and specialized proteins. New proteins, in turn, require new genetic information. Thus an increase in the number of cell types implies (at a minimum) a considerable increase in the amount of specified genetic information. Molecular biologists have recently estimated that a minimally complex single-celled organism would require between 318 and 562 kilobase pairs of DNA to produce the proteins necessary to maintain life (Koonin 2000). More complex single cells might require upward of a million base pairs. Yet to build the proteins necessary to sustain a complex arthropod such as a trilobite would require orders of magnitude more coding instructions. The genome size of a modern arthropod, the fruitfly Drosophila melanogaster, is approximately 180 million base pairs (Gerhart & Kirschner 1997:121, Adams et al. 2000). Transitions from a single cell to colonies of cells to complex animals represent significant (and, in principle, measurable) increases in CSI . . . . In order to explain the origin of the Cambrian animals, one must account not only for new proteins and cell types, but also for the origin of new body plans . . . Mutations in genes that are expressed late in the development of an organism will not affect the body plan. Mutations expressed early in development, however, could conceivably produce significant morphological change (Arthur 1997:21) . . . [but] processes of development are tightly integrated spatially and temporally such that changes early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream. For this reason, mutations will be much more likely to be deadly if they disrupt a functionally deeply-embedded structure such as a spinal column than if they affect more isolated anatomical features such as fingers (Kauffman 1995:200) . . . McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes–the very stuff of macroevolution–apparently do not vary. In other words, mutations of the kind that macroevolution doesn’t need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don’t occur.6
In short, it is plain that there is no credible evolutionary materialistic chance + necessity only dynamic process to originate cell level life systems with their functionally specified complex information far beyond the credible upper bound for random walks, from initial conditions in plausible prebiotic "soups" of whatever sort. Then, there is no credible evolutionary materialist mechanism for the onward origination of the diversity of body plans we see today and in the fossil record. In short, the evolutionary cascade from hydrogen to humans, however confidently put, rests on the a priori exclusion of intelligence -- the only known observed source of FSCI, rather than on evidence and non- question- begging logic. Students and the public have a right to know that. One that is being too often suppressed. GEM of TKI PS: Jerry -- you would be well advised to bear in mind the extraordinary degree to which contemporary modernist theology and in that general context NE archaeology is far too often driven by a priori commitments to selectively hyperskeptical, secularism-driven assumptions and assertions. (And in that context, there is a lot more archaeological support for the Bible, both NT and OT, than is likely to be admitted in today's intensely polarised, militantly secularist academic climate.)kairosfocus_{March 9, 2008
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Jerry at 162 Cook and Schoen references show declining fitness models with similar shape to the Crow declining fitness curve shown by Sanford and the declining lifespan graph shown by Sanford and above. The data is obviously from the biblical genealogies. It provides supporting evidence from ancient records - where the authors probably never dreamed about declining fitness from mutations and population genetics models. The ancient royal genealogies evidence strict verbatim oral records carried down though many generations before written documents. They provide complementary data lending credence to it.
like all oral stories probably got modified over time.
Please read these books by Cooper and Gascoine before dissing them out of hand. Why throw out the data that exists? - because it is politically incorrect? Incredulity does not invalidate the data. PD Does finding David's palace count as evidence?DLH_{March 8, 2008
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As I said a couple times I am currently reading a book by Henry Gee about the genome and in it are several things relevant to the discussion on this thread. For example, some researchers have examined in detail the gestation of the fruit fly and have correlated various parts of the genome with each development during gestation. So it does not seem there is any need to go outside the genome to seek an explanation for what happens during gestation. There is a very complicated network that ensures the gestation of the fruit fly and three researchers received the Nobel prize for analyzing this network and thousands of its interactions: Eric F. Wieschaus, Edward B. Lewis, Christiane Nüsslein-Volhard. This is part of what is known as evo devo. One interesting thing is that Gee says all the enzymes necessary for development are already in the egg before fertilization and only later will enzymes needed by transcription be created. So this sounds like everything is still within the genome for gestation since these enzymes must have originated by transcription at some time prior to fertilization. Also he implies that shape and position of the egg and later sub-divisions affects the environment and what may affect transcription at the various times of gestation. Also the number of ways that the various genes can be activated by external forces can create a very elaborate sequence of using various parts of the genome to create a myriad of effects. Someone said 2^25,000 is a lot of states and various combinations can have different effects on what is going on. So there might be enough in the genome to create an extremely complex product. But what picks the particular states or if this is really how it is done is still a mystery. So according to current theory of evolution there is no need to go to these extra dimensions as proposed by Jablonka. But the current theory is still deficient on what causes the variation and how much has actually been introduced by naturalistic means into the gene pools of populations. Based on what I am reading, this is still the achilles heel of all naturalistic views of evolution. Gee waxes on about how wonderful the whole idea of sexual reproduction is because it produces so much variety in the world and not just a series of clones that all look alike. He almost forgets he is a Darwinist and this process is blind and has no objective. He is in love with the process but does not seem to realize that this incredibly complicated system had to have someone who designed it. Natural selection and sexual reproduction are truly great design but only because someone set them up but then gave them the variation for these processes to produce all the wonderful richness we see in the world today. No natural source of variation has ever been demonstrated. Without a source of variation, natural selection and sexual reproduction might be very sterile processes.jerry_{March 8, 2008
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DLH, Recorded data by who? Do you have multiple sources for this data? When was it recorded? Where is the archeological records to back this up? I once asked a biblical scholar who was excavating sites in Israel about the stories in the bible and external sources for similar information. Specifically, about the existence of David because I thought I had recently seen something about a find that was relevant to him. She mentioned that there was a recent find of an excavation that mentioned David in it. And so far that was the only external reference to him she knew and that neither David or Solomon have little reference outside the bible. She also said there is more and more evidence for some additional events but so far the evidence is slim. So I would be careful about using a book with little outside verification as a source for anything scientific. It may go down well with Christians but not even amongst all Christians and probably not at all with the outside community. By the way I accept the bible as guide to how to lead one's life and accept the new testament as a mostly accurate description of what happened. I believe that all the people did exist and that most of the stories are probably portrayals of things that happened in the past but like all oral stories probably got modified over time. I would not use them as an accurate genealogy. The new testament was written down in the lives of the witnesses and as such has a lot more believability as to accuracy of the events. As I said a few weeks ago on another thread. I prefer Galileo's quote, that the bible tells you "How to go to heaven, not how the heavens go" nor is it the basis for any other scientific theories including the ages of the various people or the age of the earth and universe. You certainly can believe what you want, but it cannot be offered it up as science or as completely accurate history. I briefly looked at the Cook and Schoen articles and could not find anything to support your biblical chart. If you want to claim authority to the bible as as source for human life spans, you will have a very narrow audience. You will be preaching to the choir.jerry_{March 8, 2008
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Allen_MacNeill at 126
. . . we need something that could be called the “phenome”. That is, the sum total of all of the structural and functional components by means of which organisms construct and operate themselves.
Some consequences of your "phenome" focus is that there may well be variations in the "phenome" separate from the genome. Furthermore, there may well be errors in replication of the phenome independent of errors in the genome. See Jonathan Wells and Paul Nelson Homology: A Concept in Crisis Origins & Design 1997 theapologiaproject.org That gives examples of variations beyond the genome.DLH_{March 8, 2008
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Jerry at 159 Please read Sanford and address the quantitative referenced arguments he presents. This equation and graph fits the recorded lifespan data for that period up to 2100 BC, not my opinion. In terms of shape, it is very similar to Crow's fitness decline model which Sanford shows in Figure 10b. Sanford notes
Schoen et al. 1998 have modeled almost identical fitness decline curves which arise from mutation accumulation.
Crow, J. F. 1997. The high spontaneous mutation rate: is it a health risk? PNAS 94:8380-8386. Schoen, D. J. et al. 1998. Deleterious mutation accumulation and the regeneration of genetic resources. PNSAS 95:394-399. If you think the shape should be different from the historic data, or models by Crow, or Schoen et al., please provide the model and data to support it. You informally appear to refer to a later period. Greece: cf Thermistocles 525 BC Roman republic -500 BC on. If you have other data for the period before 2100 BC, please provide it. PS For further ancient records see: Mike Gascoigne History - From Creation to Modern TimesDLH_{March 8, 2008
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DLH, You are certainly entitled to your opinions. But I hope you realize that no one is going to take this seriously except those who hold a certain religious ideology. I have read several book and watched dozen of videos on ancient history in recent years and have been to Greece, Roman provinces and other places in the ancient world and not once was there any indication of unusually long life amongst anyone. There is the occasional really old person but we stil have a couple veterans from WWI. If anything the people of ancient times died young because of bad sanitation. They have documents from Greek and Roman times of families' life spans and none indicate anything any different than today. Socrates was considered an old man at 70. We are living longer today than any society in the history of mankind and people are quite active into their 70's and sometimes 80's and this is a counter trend to history. The reason for this is better nutrition, more active lives and modern medicine. I am not an expert on how mutations would have affected life spans but I would have predicted a much different chart. One that shows little degrading at first and then an accelerating effect as the mutations accumulated to drastic proportions. So I would turn your chart upside down and backwards. This would show a slow decline at first and then an accelerated decline as time went on. Such a chart does show doom and only a generation or two ahead.jerry_{March 8, 2008
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jerry at 157 Yes, please read through Sanford. In summary, Natural Selection cannot remove numerous near neutral mutations. Harmful mutations are far more prevalent than beneficial mutations. Consequently, harmful mutations accumulate as a "genetic load" decreasing fitness. Inherited diseases are one evidence of increasing degradation. e.g., see: Tay Sachs Disease at NIH & at Wikipedia Sanford cites numerous publications showing genetic evidence as well as population genetics models. Sanford's conclusion: "The Emperor has no clothes"
Careful analysis, on many levels, consistently reveals taht the Primary Axiom is absolutely wrong.
On whether Genomic Entropy exists, besides genetic evidence, Sanford graphs the biblical records of declining lifespan Y as generations X since Noah.
Fitting the data to the “line of best fit” reveals an exponential curve following the formula Y=5029.2 * X^-1.43. The curve fits the data ver well – having a correlation coefficient of 0.90. This curve is consistent with the concept of genomic degeneration caused by mutation accumulation.
A similar graph is posted at: Lifespans from Noah to Abraham http://www.worldwideflood.com/general/noahs_age_files/trend_after_noah.gif Ancient genealogies: Cooper and others have traced the genealogies of royal houses have been traced back much older than other historical records. See: After the Flood, Bill Cooper (1995 New Wine Press, PO Box 17, Chichester, West Sussex PO20 6YB England, ISBN: 1 874367 40 X) These provided ancient records that give further support to the above data.DLH_{March 8, 2008
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DLHl, What are Sanford's arguments put in simple terms? I have the book which I got 15 pages in to it and never continued. Maybe I will start it up again and see what it says. If he says that genomes are deteriorating then what evidence does he have of this outside of his own calculations? There is certainly no evidence of this in the world around us. Everything looks fit to me. Or maybe I am missing the essential message of Sanford's work.jerry_{March 8, 2008
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J at 154 Good observation on the paradox of error correction. On you query:
1. What is the ratio of beneficial mutations to detrimental but not deadly (i.e., not culled by NS) mutations?
See bornagain77's citing Sanford
"I have seen estimates of the ratio of deleterious to beneficial mutations which range from one thousand to one, up to one million to one. The best estimates seem to be one million to one (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998)
See: Gerrish, P.J., and Lenski, R. 1998, The fate of competing beneficial mutations in an asexual population. Genetica 102/103: 127-144. Bataillon, T. 2000, Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497-501. Bataillon (2000) states:
In all the studies, the mean fitness or mean of fitness related traits declined over time, suggesting that the net effect of spontaneous mutation is indeed deleterious (an exception is Shaw et al., 1999). Mean decline of the fitness components of MA lines ranged from 0.1% to 1-2% per generation.
See also: Elena, S. F. et al. 1998. Distribution of fitness effects caused by random insertion mutation in Escherichia Coli. Genetica 102/103:349-358 On your query:
2. What is the relative magnitude of the average benefit provided by a beneficial mutation in comparison to the magnitude of the average damage caused by a detrimental mutation?
Sanford in Genetic Entropy shows fitness from “benefits” to be swamped by “detrimental mutations” using literature based population dynamics models.DLH_{March 8, 2008
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Allen_MacNeill at 146
This entire discussion has circled around an elephant in the room: that fact that we are here provides prima facie evidence that there is clearly something wrong with the “genetic entropy” hypothesis (unless one agrees with Dr. Sanford that the universe and everything in it is less than 10,000 years old). IOW, as DaveScot has pointed out, there must be at least one mechanism that compensates for the surprisingly rapid decay of the genome over time.
May I encourage you to reread Sanford's arguments and reexamine your assumptions and conclusions. I read Sanford's arguments as being independent of the age of the earth. Sanford (Ch 3 p 33) cites Muller 1950 that
"one deleterious mutation per person per generation, long term genetic deterioration would be a certainty."
Sanford then cites the experimental literature showing the rates to be higher than that. Then he states (p 34)
Even if we were to accept the lowest estimate (100 mutations), and further assumed that 97% of teh genome is perfect neutral junk, this would still mean that at least 3 additional deleterious mutations are occurring per person per generation.
i.e., above Muller's critical level. As a separate complementary argument, Sanford further states:
"the human mitochondrial mutation rate has been estimated to be about 2.5 mutations, per nucleotide site, per million years. (Parsons et al, 1997) Assuming a generation time of 25 years and a mitochondrial genome size of 16,500 - this approaches one mitochondrial mutation per person per generation within the reproductive cell line Mitochondrial mutations, just by themselves, probably put us over the theoretical limit of one mutation per three children!
i.e. based on the cumulative rate of mitochondrial mutation accumulation per generation - presumably AFTER all error correcting methods.DLH_{March 8, 2008
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If the error detection and correction mechanisms are too effective, that's a problem for Darwinism, too. If genomes aren't allowed to mutate, then evolution won't occur, only recombination of existing genes. How did the genes originate? Also, the presence of error detection and correction mechanisms doesn't matter provided that they treat potentially beneficial mutations the same as potentially detrimental mutations. The real question is: Can natural selection prevent beneficial mutations from being overwhelmed by detrimental mutations? The answer to that will depend, in turn, on the answers to questions such as: 1. What is the ratio of beneficial mutations to detrimental but not deadly (i.e., not culled by NS) mutations? 2. What is the relative magnitude of the average benefit provided by a beneficial mutation in comparison to the magnitude of the average damage caused by a detrimental mutation? And in the final analysis, if one was to suppose materialism, it seems the answer to such questions would be a function of how "lucky" the universe is.j_{March 8, 2008
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jerry (#150): It is true that spermatogenesis is constantly active during reproductive life, but that does not necessarily mean that a lot of cell divisions take place. Indeed, the final part is similar both for oogenesis and spermatogenesis (one mitosis and two meiosis). Spermatogenetic cells, like other actively differentiating cell compartments (hemopoiesis is a good example) are maintained from a higher stem cell compartment (spermatogonia). Stem cell compartments are usually characterized by two properties: self-maintenance and ability to differentiate. In other words, a stem cell compartment is usually small (few cells), and may have a very slow reproductive activity, but that activity realizes two different tasks: providing differentiating cells for the downstream differentiation, and at the same time maintain the number of undifferentiated precursors. Anyway, as certainly many more spermatocytes are producted in the reproductive life of a male than oocytes in a woman, it is certainly possible that the spermatocytic compartment undergoes a higher number of cell divisions. It could be interesting to observe that other factors can certainly influence genetic errors, beyond the number of cell divisions. In particular, especially in oocytes, the age of the cell is known to be an important risk factor for chromosomal abnormalities, even if all oocytes undergo the same number of cell divisions. Regarding the ability of cells, at least in humans, to check for erros in DNA duplication, that is a well established fact. Various checkpoints are known in cell cycle, where specific molecules (usually extremely important also in carcinogenesis) can stop the cycle to allow that the cell may "correct" some genetic error generated in DNA duplication, or start the process of apoptosis (controlled death) if the errors couldn't be repaired. That is well known. Anyway, I don't think that we really know "how" those checkpoints and molecules "recognize" errors. That is a very interesting field of research, and it is certainly being extensively worked out, also because of its important implications in medicine, especially for cancer. But the answers are probably still very far away.gpuccio_{March 7, 2008
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